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机构地区:[1]南华大学心血管疾病研究所动脉硬化学湖南省重点实验室 [2]南华大学医学院诊断学教研室,湖南省衡阳市421001
出 处:《中国动脉硬化杂志》2014年第3期233-236,共4页Chinese Journal of Arteriosclerosis
基 金:湖南省研究生科研创新项目(2012SCX13)
摘 要:目的观察载脂蛋白AⅠ(ApoAⅠ)对脂多糖诱导的巨噬细胞源性泡沫细胞炎症因子表达的影响,探讨锌指蛋白(TTP)翻译后修饰在ApoAⅠ抑制泡沫细胞炎症因子表达中的作用。方法 THP-1巨噬细胞源性泡沫细胞以ApoAⅠ和/或脂多糖处理,采用ELISA检测细胞裂解液中炎症因子白细胞介素1β(IL-1β)蛋白表达;采用实时定量PCR检测IL-1βmRNA表达和降解率;采用Western blot检测TTP和磷酸化TTP(p-TTP)的表达。结果 ApoAⅠ明显抑制脂多糖诱导泡沫细胞炎症因子的表达,并影响TTP表达和TTP去磷酸化。结论 ApoAⅠ抑制泡沫细胞炎症因子表达机制涉及TTP的去磷酸化,与TTP促进含有腺苷酸环尿苷酸丰富的元件(ARE)的mRNA降解有关。Aim To observe the effect of apolipoprotein A Ⅰ ( ApoA Ⅰ) on the expression of inflammatory cytokines and explore the role of tristetraprolin (TrP)-translational modification in the ApoA Ⅰ inhibition macrophage-derived foam cells expression of inflammatory cytokines. Methods THP-1 macrophage-derived foam cells were treated with ApoA I and/or lipopolysaccharide(LPS). Enzyme linked immunosorbent assay was used to determine levels of interleukin-1β (IL-1 β) in cell lysates. Real-time polymerase chain reaction was used to determine mRNA and degradation rate of IL-1β. Western blot was used to determine protein levels of TIP and p-TIP. Results ApoA I significantly inhibited the levels of LP3- induced macrophage-derived foam cells inflammatory cytokines, and influenced the expression of TIP and TIP dephosphoryla- tion. Conclusion ApoA I inhibiting the expression of inflammatory cytokines in macrophage-derived foam cells may be involved in the dephosphorylation of TIP, which can bind and target ARE-containing mRNA for rapid degradation.
关 键 词:锌指蛋白 载脂蛋白A Ⅰ 巨噬细胞源性泡沫细胞 炎症因子
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